2. Academic Validation
  3. Icaritin protects against airway inflammation by inhibiting the TLR4/NF-κB pathway in vivo and in vitro

Icaritin protects against airway inflammation by inhibiting the TLR4/NF-κB pathway in vivo and in vitro

  • Pulm Pharmacol Ther. 2025 Sep:90:102380. doi: 10.1016/j.pupt.2025.102380.
Bo Xiao 1,  Guiming Zhou 2,  Lixia Hou 2,  Lihong Yang 3,  Zhimei Li 3,  Yuchun Cai 3,  Ailing Zhao 3,  Biwen Mo 4,  Dong Yao 5
Affiliations

Affiliations

  • 1 Department of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Guilin Medical University, 541199, Guilin, China; The Laboratory of Respiratory Disease, Affiliated Hospital of Guilin Medical University, Guilin, 541000, China; Department of Pulmonary and Critical Care Medicine, Affiliated Hospital of Guilin Medical University, Guilin, 541000, China.
  • 2 The Laboratory of Respiratory Disease, Affiliated Hospital of Guilin Medical University, Guilin, 541000, China; Department of Pulmonary and Critical Care Medicine, Affiliated Hospital of Guilin Medical University, Guilin, 541000, China.
  • 3 The Laboratory of Respiratory Disease, Affiliated Hospital of Guilin Medical University, Guilin, 541000, China.
  • 4 Department of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Guilin Medical University, 541199, Guilin, China; Guangxi Clinical Research Center for Diabetes and Metabolic Diseases, Guangxi Health Commission Key Laboratory of Glucose and Lipid Metabolism Disorders, The Second Affiliated Hospital of Guilin Medical University, 541199, Guilin, China; Guangxi Key Laboratory of Metabolic Reprogramming and Intelligent Medical Engineering for Chronic Diseases, The Key Laboratory of Respiratory Diseases, Education Department of Guangxi Zhuang Autonomous Region, Guilin Medical University, 541000, Guilin, China. Electronic address: 1042587352@qq.com.
  • 5 Department of Respiratory and Critical Care Medicine, Second Affiliated Hospital of Guilin Medical University, 541199, Guilin, China; Guangxi Clinical Research Center for Diabetes and Metabolic Diseases, Guangxi Health Commission Key Laboratory of Glucose and Lipid Metabolism Disorders, The Second Affiliated Hospital of Guilin Medical University, 541199, Guilin, China; Guangxi Key Laboratory of Metabolic Reprogramming and Intelligent Medical Engineering for Chronic Diseases, The Key Laboratory of Respiratory Diseases, Education Department of Guangxi Zhuang Autonomous Region, Guilin Medical University, 541000, Guilin, China. Electronic address: dong.yao@glmc.edu.cn.
PMID: 40743986 DOI: 10.1016/j.pupt.2025.102380
Abstract

Icaritin, a bioactive phytomolecule derived from Epimedium Flavonoids (EFs), has been shown to have anti-inflammatory, anti-proliferative, and pro-apoptotic properties. However, its potential mechanisms in asthma airway inflammation have not been elucidated. In this study, Ovalbumin (OVA)-induced asthma mouse model and human bronchial epithelial cells (BEAS-2B) were used to illustrate the effects and mechanisms of Icaritin on airway inflammation. Specific airway resistance (sRAW) was used to detect the airway hyperresponsiveness (AHR). Hematoxylin-eosin (H&E) and periodic acid schiff (PAS) were used to detect the pathological changes. Bronchoalveolar lavage fluid (BALF) was used to detect the airway inflammatory cells. Serum and supernatants were used to detect the cytokines. Immunohistochemistry (IHC) and western blotting were used to detect the expression of TLR4, p-65, p-p65, IκBα, and p-IκBα. Cell Counting Kit-8 (CCK-8) was used to detect the cell viability. Icaritin suppressed AHR, attenuated eosinophilic infiltration and mucus hypersecretion, and significantly reduced the levels of OVA-specific cytokines in asthmatic mice. Moreover, Icaritin inhibited TLR4 expression, decreased phosphorylation of IκBα, and reduced NF-κB p65 activation in lung tissue of asthmatic mice. Further mechanistic studies showed that Icaritin reduces TLR4-induced inflammatory factor expression and blocks TLR4-activated NF-κB pathway in BEAS-2B cells. These findings demonstrate for the first time that Icaritin suppresses airway inflammation in asthma by inhibiting the TLR4/NF-κB pathway, suggesting its potential as a therapeutic agent for asthma.

Keywords

Airway inflammation; Asthma; BEAS-2B cells; Icaritin; TLR4/NF-κB signaling pathway.

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